Ernesto Pollitt and Nita Lewis
Human Nutrition Center, School of Public Health, University of
Texas, Houston, Texas

INTRODUCTION

The purpose of this paper is to depict the role of nutrition
as a determinant of formal educational achievement. First, an
evaluation is made of the role of nutrition in shaping aptitudes
and abilities of the pre-school child. A basic educational
proposition is that school success will depend, in part, on the
capabilities of the student at the beginning of his formal
education (1). The paper also looks at the role of nutrition once
the child is in school. Accordingly, from a longitudinal
perspective, the substantive difference between these two periods
lies in their focus on the developmental implications when the
nutrition variable affects the child.

Somewhat arbitrarily, a distinction is made between possible
behavioural effects of malnutrition, i.e., iron deficiency or
protein-energy malnutrition (PEM), and the co-variations that may
be established between nutritional and behavioural indicators in
populations where malnutrition is not a major public health
problem. Part I of this paper deals with the former and Part II
will deal with the latter. This distinction exemplifies the
differences in the concerns of developing countries and those of
the industrialized countries.

Neither part presents an exhaustive review of the literature.
Studies are often selectively cited to substantiate statements
made; in other instances (especially when the focus is on areas
where there is scarcity of information) studies are reviewed in
some detail. Also, it should be pointed out that the issue of
mechanisms whereby nutrition factors offset behaviour is not
discussed.

INFANCY AND THE PRE-SCHOOL PERIOD- NUTRITIONAL
DEFICIENCIES

In this section the focus is restricted to highly prevalent
forms of malnutrition, mostly in developing countries, and for
which evidence of an impact of malnutrition is established or
suggested. Specifically, the association between behaviour and
the nutritional anomalies of protein-calorie malnutrition, iron
deficiency and anaemia, iodine deficiency, and avitaminosis A are
discussed.

Protein-Energy Malnutrition (PEM)

"Most children with PEM are generally born into, and
develop in, an unsanitary environment with few early
opportunities for learning and psychosocial stimulation, and are
constantly exposed to agents that will lead to infectious
diseases" (2). Because of the total impact of the
environment on development, individuals with a history of
malnutrition are likely to have specific deficiencies in
cognitive function or learning ability (for detailed literature
reviews, see 3, 4). The isolation of specific PEM effects on
cognition has been a troublesome methodological problem.

From the available published information, the following
inferences are warranted.

Severe PEM occurring throughout most of the first two
years of life in children living in populations where
malnutrition is endemic generally results in severe
cognitive deficits (5 9). In the absence of an
appropriate rehabilitation programme (10, 11) or change
to a stimulating home environment (12), this deficit will
restrict the chances that the child has of taking
advantage of the formal educational system (13 - 19).

Severe PEM secondary to a biological disorder (e.g.,
pyloric stenosis) during the first two years of life in
children not exposed to poverty conditions may, but
generally does not, leave cognitive deficits that
interfere with school learning (20 - 23).

Infants and young children of comparatively short stature
(an indicator of nutritional history) within populations
where malnutrition is endemic are likely to perform less
well than children of average height from the same
community on tests of intelligence or on tests of
specific cognitive processes (24, 25). Accordingly, their
school achievement will probably not be up to the level
of their comparatively taller peers from the same
populations (26).

Infants and pre-school children with a history of
moderate to severe malnutrition who are exposed to
stimulating home environments (12), or to long-term
nutrition and psychosocial stimulation programmes may be
partly, if not totally, rehabilitated from their
cognitive deficits (10, 11, 27). Although data supporting
this issue are not yet available, the rehabilitation may
be successful enough to expect them to compete
satisfactorily with their peers in school.

Iron Deficiency and Anaemia

Data from two recent experimental studies indicate that in
preschool children, particular process features of cognition,
such as selective attention, vigilance, or rehearsal strategies
for memory function, may be altered by iron deficiency with (28)
and without anaemia (29). (For detailed review of literature, see
30.) The study of Pollitt, et al. (29) suggests that there may be
some adverse functional consequences in cases of mild iron
deficiency, which were previously identified as falling within
the normal variability of iron status in children. Oski and Honig
(28) and Pollitt, et al. (29) found that iron-repletion therapy
was followed by a reversal of all previously detected cognitive
deficits.

It may be inferred that the iron-deficient pre-school child
will not have learning difficulties once he or she reaches the
school setting if the sideropenia is reversed. On the other hand,
these data suggest that school-age children may have learning
difficulties if they are iron-deficient (see the section on iron
deficiency in the school-age child in Part II of this paper).

One other developmental issue that requires further research
is whether long-term, chronic iron deficiency during the first
year of life can have long-lasting effects. The experimental work
cited above does not address the issue of the timing of the
deficiency. One study investigated possible long-term effects of
iron deficiency (31). In a sample of 61 children, 32 developed
iron-deficiency anaemia between six and 18 months of age (Hb.
6.1- 9.5 g/dl). Twenty-nine infants received neonatal iron
dextran injections and were not anaemic (Hb. 11.5- 23.9 g/dl)
during this age period. Neurological evaluation performed six or
seven years later showed that the iron-deficient group had more
"soft neurological signs" than found in the controls.
Unfortunately, because these data were presented in an abstract,
there is no way of critically assessing the soundness of the
study design and findings.

Iodine Deficiency

Severe iodine deficiency results in hypothyroidism, a
pathological state characterized by an impairment in synthesizing
thyroid hormone. Unless the thyroid gland is nonfunctional or
absent, the impairment is accompanied by goitre, or thyroid gland
enlargement, which results from hyperstimulation of the thyroid
gland. Severe endemic goitre- which is generally the result of a
diet deficient in iodine (32)- has been clearly associated with
endemic cretinism in different world regions (33, 34). A cretin
is characterized by severe intellectual retardation, dysarthria,
and possibly deafness. With few, if any, exceptions, cretins are
not able to attend school because of their severe intellectual
limitations. They represent the most dramatic example of the way
a nutritional deficiency may stop a child from taking advantage
of the formal educational system (34).

A continuum of neurological impairment resulting from iodine
deficiency has also been postulated. One end-point of the
continuum is cretinism, while the other extreme is a milder
neurological impairment (35). Although little argument exists
about the association between goitre and severe mental
retardation and cretinism, there is considerable controversy
about the validity of the the continuum hypothesis.

Evidence recently accumulated from studies on the effect of
iodized oil on pregnant women in populations with a high
prevalence of iodine deficiency provides some support for the
continuum hypothesis (36, 37). These data also suggested that the
adverse effects of iodine deficiency on the central nervous
system begin in the early stages of foetal life.

In Ecuador, a study was conducted comparing the IQs of
children in two communities (37). In one, iodized oil was
injected into every member of the community; the other community
served as a control. Children in the treatment community were
selected for the study if they were at least 36 months old, and
if treatment of their mothers had occurred either prior to
conception or between the fourth and fifth months of foetal life.
They were then matched by age and sex with children from the
non-treated population. The difference in the Stanford Binet IQ
for the children of the mothers treated during gestation and the
controls was not statistically significant. On the other hand,
the mean IQ for the offspring of the women treated prior to
conception was much higher and statistically different from that
of controls. Treatment, therefore, had a differential effect on
intelligence dependent on its timing.

When it was initiated during the second trimester of
pregnancy, it did not appear to prevent mild intellectual
retardation in the offspring. Conversely, it had a demonstrably
salutary effect when it was given before embryogenesis.

Although it is now possible to eradicate iodine deficiency and
goitre in most populations (32) through appropriate prophylactic
programmes, this specific nutritional deficiency still represents
a major public health problem (38).

Vitamin A and Xerophthalmia

Vitamin-A deficiency causes abnormalities in tissue metabolism
and resultant weight loss, nervous disorders, reduced resistance
to infection, and eye lesions that progressively worsen until
blindness occurs (see 39, p.5). These lesions, xerophthalmia and
kerotomalacia, are most frequently found in young children and
are often accompanied by protein-energy malnutrition. Lesions
form on the eyes after the fluids that lubricate the conjunctiva
dry up. This process is reversible by treatment with vitamin A.
Left untreated, however, the condition worsens until the eyes are
irreversibly blind.

From the data available, it appears that of the survivors of
severe xerophthalmia, 25 per cent are totally blind, 50 to 60 per
cent are partially blind, and 15 to 25 per cent have unimpaired
sight. Data sources are such that the total annual number of
cases of blindness resulting from xerophthalmia is impossibie to
determine (39, p.9). A first estimate of 20,000 per year by
McLaren (40) was raised to 100,000 per year in 1970; but this
figure has yet to be confirmed (39).

The effects of the blindness resulting from xerophthalmia on a
child are self-evident. Loss of vision is a severe handicap to
the individual and to the family. To our knowledge, no studies
have been done to determine how many children never attend school
as a result of xerophthalmia, or how school performance is
affected by varying degrees of visual handicap.

CONCLUSION

The data reviewed here have shown that nutrition factors
should be considered as inputs in the educational attainment
process of children. These inputs can be defined in connection
with the timing of their effects. They may affect aptitudes and
abilities of pre-school children, and determine in part the
degree of success the child will have later within the school.
They may also affect the student directly once he/she is embarked
upon formal education.

In the pre-school period, nutritional deficiencies may become
sufficient causes for the exclusion of the child from
participating in the regular school system (e.g., cretinism and
xerophthalmia secondary to endemic iodine and vitamin-A
deficiency, respectively). PEM generally is not a sufficient
cause of cognitive derangements, but it is often a substantive
component of a sufficient cause. When PEM (and possibly
iron-deficiency anaemia) is part of an economically impoverished
environment, the probabilities are very high that the cognitive
competence of a child will be adversely affected. In the absence
of appropriate rehabilitation his or her future school
performance will not be satisfactory, or at least not up to the
level of peers.

Once the child is in school, iron deficiency can affect his or
her cognitive function. Specifically, it can interfere with
selective processes, such as attention, vigilance, or rehearsal
strategies for memory operations. Yet it is not known whether
these effects restrict learning ability. At best, a probability
statement can be advanced indicating that in the presence of iron
deficiency the likelihood of successful school achievement is
decreased.

REFERENCES

1. L. Alexander and J. Simmons, "The Determinants of
School Achievement in Developing Countries: The Educational
Production Function," International Bank for Reconstruction
and Development, Staff Working Paper No. 201 (Washington, 1975).

37. R. Fierro-Benítez, l. Ramírez, E. Estrelia, and J.B.
Stanbury, "The Role of Iodine in Intellectual Development in
an Area of Endemic Goiter," in J.T. Dunn and G.A. Medeiros,
eds., Endemic Goiter and Cretinism: Continuing Threats to World
Health (Pan American Health Organization, Washington, 1974).